Truelearn Flashcards
How to calculate PAO2 from a given PACO2?
PAO2 = FiO2(PB – PH2O) – PCO2 / RQ
PAO2 = alveolar oxygen partial pressure FiO2 = fraction of inspired oxygen PB = barometric pressure PH2O = vapor pressure of water RQ = respiratory quotient
PAO2 = 0.21 (760 – 47) – PACO2/0.8 ((((((((PAO2 = 150 - PACO2/0.8)))))))
what is the relation between fraction of inspired O2 (FiO2) to pressure inspired oxygen (PiO2)?
PiO2 = FiO2 x (PBar - PH2O).
If PBar and PH2O remain constant, PiO2 and FiO2 are directly proportional.
PiO2 = Pressure of inspired oxygen equation?
PiO2 = FiO2 * (PBar - PH2O)
FiO2 = Fraction of inspired oxygen PBar = Barometric pressure (760 mm Hg at sea level) PH2O = Vapor pressure of water (47 mm Hg at sea level)
What is Fraction of inspired oxygen (FiO2)
is the fraction of oxygen in the volume being measured.
Right shift of O2 dissociation curve causes? (Increased P50)
Acidosis, hypercarbia, hyperthermia, increased 2,3-DPG.
Shift “RIGHT”: (R)ise In 2,3-DP(G), (H+), and (T)emp.
The oxygen affinity for hemoglobin is … (P50 is …) in children than in adults
Lower. and higher P50.
The term P50 is designated as the partial pressure of oxygen (in mm Hg) when oxygen saturation (SaO2) is 50%. In a normal adult, P50 is 27 mm Hg. When the oxyhemoglobin dissociation curve shifts to the left or to the right, P50 will decrease or increase respectively. Thus, P50 can be used to relate the oxygen affinity for hemoglobin.
Why ptn with dependent hypoxia respiratory drive (COPD) May have a PaO2 ~60 without changes in ventilation?
Because the carotid body chemoreceptors sends signals through gloss pharyngeal nerve when PaO2 below 100 but it won’t change ventilation until PaO2 is <60
Pathway of peripheral chemoreceptors hypoxic ventilation drive?
Decrease in PaO2 (not PAO2) will sense the carotid body sinus, fires glossophqryngeal nerve afferent signaling to CNS ventilation centers.
This is inspired by opioids, BZDs, volatiles and b/l carotid endarterectomy
Pathway of central chemoreceptors increasesing reapiration?
They are located in ventral medulla. They sense the increase in H+. (The increase CO2 has the ability to cross BBB (not PaCO2) which then converted to carbonic acid by carbonic anhydride and therefore the increase H increases RR and TV (CO2 -> H2CO3-> H+ -> inc RR and TV).
The systemic met acidosis dose not have the same effect as H+ don’t cross BBB (it’s CO2 that cross BBB)
Factors shifts the CO2 ventilator response curve to left?
Arterial hypoxemia Metabolic academia Surgical stimulation Fear/anxiety Increased ICP
All cause hyperventilating (increases MV with decreasing PaCO2 on curve slope).
Factors shifts CO2 ventilators response curve to right?
Opioids
Barbiturates
Sedatives
Volatiles < 1 MAC
Relationship of pH and PaO2 with Temp
pH inversely to Temp
PaO2 directly to Temp
Direct/indirect hypoxic plum vasoconstrictor inhibitors? (Factors opens up for blood to flow to poorly ventilated lung segment)
Hypocarbia, vasodilator, infection, met alkalosis, gas MAC>1
Indirect associated with increase plum artery pressure; hypervolemia, vasoconstrictor, hypothermia, thrombosis, large hypoxic lung segment
What it effected expiatory/inspiratory loop in intrathoracic obstruction on flow-volume loop?
Intrathoracic obstructions alter the expiratory curve.
(During expiration, intrathoracic pressure becomes positive which further decreases the airway diameter, enhances the degree of obstruction, and impairs airflow.)
What it effected expiatory/inspiratory loop in extrathoracic obstruction on flow-volume loop?
extrathoracic obstructions alter the inspiratory curve.
During inspiration, the negative inspiratory pressure causes the obstruction to increase.
what are causes of plateaued and decreased inspiratory and expiratory on flows-volume loop
A fixed upper airway obstruction or fixed large airway obstruction (e.g., foreign body, tracheal stenosis, large airway tumor) which impairs BOTH inspiration and expiration
The flow-volume loop in a patient with COPD is characterized by …
expiratory phase with a quick peak followed by a much lower than normal plateau phase
Functional residual capacity is the sum of the expiratory reserve volume and residual volume. It is reduced by …
obesity, in females (10% less than males), and when transitioning from upright to supine, prone, or Trendelenburg position.
Interestingly, there is no significant change in FRC as position changes from 0° to Trendelenburg of up to -30°. However, beyond -30°, the drop in FRC is considerable.
A large difference between peak and plateau pressure is suggestive of
If the peak and plateau pressure are not significantly different (normal is 4-10 cm H2O), it suggests an issue with
high airway resistance. Associated conditions such as bronchospasm, kinked endotracheal tube, and mucus plugging should be evaluated and treated.
respiratory compliance such as poor positioning, pulmonary fibrosis, pneumothorax, obesity, or chest wall deformity or compression.
Physiological changes occur with insufflation of abdomen by laprascopic
Decreases lung compliance and increases PIP
Increase V/Q mismatch due to atelectasis and decreases FRC
Elevated CO2 due to CO2 insufflation and decreases lung perfusion and ventilation
PiO2 is the partial pressure of O2 at room air
PAO2 partial pressure of O2 in alveolar equation
PiO2 = (barometric pressure - H2O vapor pressure) x FiO2
PiO2 - (PaCO2/R)
RS system compliance formula?
1/CRS = 1/CL + 1/CCW
Where C is compliance, RS is respiratory system, L is lungs, and CW is chest wall.
Myocardial oxygen supply is affected by …
1) Coronary perfusion:
CBF = (AoDP – LVEDP) / CVR.
2) oxygen content; mainly HR and Hgb
CaO2 = (Hgb * 1.34 * SaO2) + (0.003 * PaO2)
Oxygen dissolved in arterial blood (0.003 x PaO2) raises the total value by only a small amount, therefore its neglected.
Left ventricular systolic pressure affects myocardial oxygen demand or CBF?
myocardial oxygen demand.
has no affect on myocardial O2 supply.
